Pathophysiology Of Urinary Tract Obstruction - Campbell's 37

Front 1

What happens to GFR and Renal Pelvic Pressure with unilateral ureteral obstruction?

Back 1

Animal experiments have demonstrated a triphasic pattern of RBF and ureteral pressure changes in UUO
that differs from BUO or unilateral obstruction of a solitary kidney (Fig. 37-1). With UUO, RBF increases
during the first 1 to 2 hours and is accompanied by a high PT and collecting system pressure because of the
obstruction. In a second phase lasting 3 to 4 hours, these pressure parameters remain elevated but RBF begins to
decline. A third phase beginning about 5 hours after obstruction is characterized by a further decline in RBF, now paralleled by a decrease in PT and collecting system pressure. These changes are explained by physical
alterations in flow dynamics within the kidney and are modified by changes in the biochemical and hormonal milieu regulating renal resistance

Front 2

What are the hemodynamic changes associated with bilateral ureteral obstruction?

Back 2

The changes with BUO or obstruction of a solitary kidney are different. In contrast to the early robust renal
vasodilation with UUO, there is a modest increase in RBF with BUO lasting approximately 90 minutes
followed by a prolonged and profound decrease in RBF that is greater than that found with UUO

Front 3

How does the distribution of blood flow in the kidney differ with unilateral ureteral obstruction from bilateral ureteral obstruction?

Back 3

the shift seen with UUO of blood flow from outer to inner cortex is the opposite with BUO.

Front 4

Why does ureteral pressure remain elevated longer in bilateral ureteral obstruction compared to unilateral ureteral obstruction?

Back 4

Ureteral pressure remains high because BUO passes through a phase of
preglomerular vasodilation and then a prolonged postglomerular vasoconstriction. This explains the persistent
elevation in ureteral pressure in spite of a decrease in RBF and increase in renal resistance. In contrast, in UUO
the initial preglomerular dilation and short-lived postglomerular vasoconstriction are followed by a more prolonged
preglomerular vasoconstriction that tempers elevations in PGC and hence in PT. This difference between the two
pathophysiologic conditions has been hypothesized to be due to an accumulation of vasoactive
substances in BUO that could contribute to preglomerular vasodilation and postglomerular
vasoconstriction. Such substances would not accumulate in UUO as they would be excreted by the
contralateral kidney. Atrial natriuretic peptide (ANP) appears to be one of these substances

Front 5

Why is there an elevation in ANP levels in bilateral ureteral obstruction?

Back 5

With excretory ability abrogated, BUO increases intravascular volume, as evidenced by an increase in
pulmonary capillary wedge pressure and body weight, which serves as the stimulus for secretion of ANP. ANP
increases afferent arteriolar dilation and efferent arteriolar vasoconstriction, thus increasing PGC. It also decreases
the sensitivity of tubuloglomerular feedback, inhibits release of renin, and increases Kf

Front 6

Where is the ejaculate made from?

What is the "pre-ejaculate?"

Back 6

Secretions from the testis, epididymis, bulbourethral glands (Cowper's glands), glands of Littre (periurethral
glands), prostate, and seminal vesicles compose the normal seminal fluid. The fluid is released from the glands in a
specific sequence during ejaculation. Before the ejaculation of the major portion of the ejaculate, a small amount of
fluid from the glands of Littre and the bulbourethral glands is secreted. This is followed by a low viscosity opalescent
fluid from the prostate containing a few sperm. The principal portion of the ejaculate contains the highest
concentration of sperm, along with secretions from the testis, epididymis, and vas deferens, as well as some prostatic
and seminal vesicle fluids.

Front 7

What is ddx for small volume ejaculate?

Back 7

Small volume ejaculates may be produced in patients with obstruction of the ejaculatory ducts, androgen
deficiency, retrograde ejaculation, sympathetic denervation, absence of the vas deferens and seminal
vesicles, drug therapy, or bladder neck surgery.

Front 8

What is necrospermia?

Back 8

Alternatively, nonmotile sperm may be dead, in which
instance the patient is said to demonstrate necrospermia.

Front 9

What is WHO criteria for normal semen analysis?

Back 9

*Volume is 2.0ml or more
*pH is 7.2 or greater
*Sperm concentration is 2.0x10 to the 6/ml
*Motility is 50% A or B or 25% with all A motility
*Morphology 15% or greater normal by strict criteria
*Viability 75% or greater